DOES RESUSCITATION PRODUCE A REPERFUSION INJURY

Conceptually, shock with resuscitation should produce cellular changes that parallel those observed in a single organ exposed to ischemia wi th reperfusion, i.e., a transient worsening of the injury pattern afte r reperfusion with the degree of recovery reflecting the magnitude of the ischemic injury. To test this hypothesis, 74 male Sprague Dawley r ats (300-400 g) were randomized into two groups with controls and expo sed to 1) hemorrhagic shock (mean arterial pressure <50 mm Hg) for 2 h ours before sacrifice, or 2) shock (2 hours) with reinfusion of shed b lood over 1 hour before sacrifice. Mean arterial pressure, blood loss, serum lactate, base excess, and bicarbonate were serially measured to determine the degree of tissue ischemia. At sacrifice, hepatic mitoch ondrial function was determined by the respiratory control ratio. Our findings were as follows: 1) Hemorrhagic shock produced significant (P < 0.001) tissue ischemia and impairment of mitochondrial function (P ( 0.001), 2) resuscitation rapidly corrects the metabolic sequelae of tissue ischemia, and 3) mitochondrial function was unaffected by resus citation. We conclude that resuscitation rapidly corrects the tissue i schemia associated with hemorrhagic shock, without producing any measu rable reperfusion injury at the mitochondrial level.